Any device intended to control hemodynamics of the circulatory system in patients with cardiac injury or disease requires a mechanism for efficiently assessing the patient's hemodynamic status. The performance of the heart's left ventricle is a primary determinant of hemodynamic status. The measurement of blood pressure within the left ventricle would accurately provide a parameter directly related to left ventricular function. However, there is no practical means for measuring pressure within the left ventricle. The measurement of blood pressure within the peripheral systemic circulatory system provides some assessment of left ventricular performance. Unfortunately, this measurement is inaccurate due to the unstable nature of detected blood pressure resulting from peripheral and ancillary influences such as differences in the contractility of peripheral blood vessels. More accurate information regarding left ventricula function is provided by combining blood pressure measurements from the peripheral circulatory system with those from either of the right chambers of the heart.
The heart may be more accurately modelled as a constant volume pump than as a constant pressure pump. Therefore, a better criterion for assessing the hemodynamic status of the circulatory system is provided by measurements of the volume of blood flow pumped from the heart, rather than blood pressure determinations. In a constant volume system, the parameters of end diastolic volume, ventricular filling, cardiac output, and the contractility of the heart muscle accurately describe the pumping performance of the heart. Each of these parameters is directly related to cardiac contractility. The primary parameter of interest in a hemodynamic control system is, therefore, myocardial contractility. In the present invention, myocardial contractility is measured directly, by detecting the motion of cardiac myofibrils within the heart muscle. One technique, herein disclosed, for evaluating the motion of cardiac myofibrils involves Doppler ultrasound sensing using a transducer. The transducer is implanted into the right ventricle within a patient's heart with its ultrasonic beam directed into the septum separating the right ventricle from the left ventricle. Implantation of the ultrasound transducer in the right ventricle permits access to the heart using medical procedures which are standard in the fields of electrophysiological testing and cardiac pacing.
Contractility of the cardiac myofibrils determines the forces and pressures generated within the heart. As the heart muscle contracts, the pressure increases within the chambers of the heart. In turn, the changes in pressure control the opening and closing of the heart valves and regulate the blood flow between chambers and out of the heart, into the aorta and the systemic and pulmonary circulatory systems. Measurement of the velocity of motion of cardiac myofibrils is a fundamental measurement of myocardial contractility. This measurement is free from extraneous sources of error. By determining cardiac contractility directly, a cardiac assist device can accurately assess whether the cardiovascular system is adequately supporting the needs of the body. Such a device can use the cardiac contractility measurement as a control variable in a closed-loop hemodynamic control system. Other prior art control parameters are less directly related to the response of the heart since they attempt to characterize cardiac function from measurements secondarily related to hemodynamics.
The fundamental advantage of a hemodynamic control method based on the measurement of cardiac contractility or its direct corollary, cardiac output, and its usage to control a cardiac assist device is illustrated by the three-phase relationship between cardiac output and pacing rate shown in a report by J. L. Wessale et al., entitled "Cardiac Output Versus Pacing Rate At Rest And With Exercise In Dogs With AV Block", PACE, Vol. 11, page 575 (1988). At low pacing rates (first phase), the cardiac output increases proportional to pacing rate. At some point (second phase), further increases in pacing rate cause the cardiac output to rise only slightly, if at all. At still higher pacing rates (third phase), further increases will cause the cardiac output to diminish. The width of the second phase is considered an indication of the pumping capacity of the ventricles and the health of the heart. Rate-responsive pacemakers cannot determine the phase of the cardiac output/pacing rate relationship for a given pacing rate without measuring cardiac output.
Some prior art devices measure physiological and physical parameters other than cardiac contractility, and regulate hemodynamics accordingly. Hemodynamic control in such devices is performed in an open-loop, rather than a closed-loop, manner since the relationship between the actual hemodynamic state, as defined by the cardiac contractility, and the measured control parameter is not known. The response of such devices is less directly related to the response of the heart since the hemodynamic status is characterized by a parameter related only secondarily to such status. The prior art includes a number of pacemakers, called rate-responsive pacemakers, each of which adjusts the heart rate of a patient based on a measurement acquired using a sensor to derive a parameter related in some manner to metabolic demand. Cardiac electrical activity (either stimulated or natural), body motion, respiration and temperature are examples of such parameters for assessing metabolic demand in a cardiac control device.
The method of determining metabolic demand using each of these measured parameters requires the previous correlation of the parameter with cardiac output by means of clinical experimentation. These correlation relationships are subject to wide variability from patient to patient and from one test to the next in an individual patient. More importantly, each of the parameters is subject to influences from physiological and physical sources which are unrelated to cardiac output and metabolic demand. The influences affecting these measurements are poorly understood and difficult to characterize. Furthermore, since the secondarily-related metabolic indicator pacing rates do not take the actual output from the heart into account, they may actually hinder the ability of the heart to meet the necessary metabolic demand, as illustrated in the aforementioned report by Wessale. As a consequence, all sensing and control means using a control parameter which is secondarily related to cardiac output and metabolic demand suffer from the inability to assess the hemodynamic status of the cardiovascular system.
It is known in the prior art of cardiac pacemakers to control pacing rate based on the determination of cardiac output. In one example (Salo et al. U.S. Pat. No. 4,686,987, entitled "Biomedical Method and Apparatus for Controlling the Administration of Therapy to a Patient in Response to Changes in Physiological Demand", issued Aug. 18, 1987), the device estimates cardiac output using intracardiac impedance measurements between two spaced electrodes disposed within the right ventricular cavity. This apparatus measures the tissue impedance by injecting subthreshold (non-stimulating) electrical current pulses into the body through one electrode and detecting the current at the second electrode. From changes in impedance, this device estimates changes in left ventricle volume by integrating the measurements over time, leading to the estimation of cardiac output. Unfortunately, inherent in the usage of impedance as a control parameter is the lack of a reliable relationship between impedance and actual cardiac output sought as the basis for control. When a device measures impedance using only two electrodes, gross volume approximation errors occur which are magnified during the integration process leading to the determination of cardiac output. In addition, since the electrodes are necessarily implanted into the right rather than the left ventricle (the left ventricle is not available for access) and the estimate of left ventricular volume in this manner is very crude and inaccurate, the cardiac output estimate derived using impedance techniques is highly susceptible to cumulative erors in each of the integration steps. Furthermore, extraneous influences on the impedance signal such as noise from respiration, changes in the patient's posture, and electrical interference produce a large noise signal and lead to further errors.
It is also known in the art to use noninvasive Doppler ultrasound techniques to measure the maximum blood flow velocity in the aorta or pulmonary artery and to determine cardiac output as a product of the time average mean velocity and the estimated crosssectional area. One such usage of Doppler ultrasound techniques is described by Colley et al. in U.S. Pat. No. 4,319,580, entitled "Method for Detecting Air Emboli in the Blood in an Intracorporeal Blood Vessel", issued Mar. 16, 1982. Devices use these prior art ultrasound techniques to monitor cardiovascular hemodynamics by measuring cardiac output and stroke volume, but do not use these measurements to control cardiac functions.